Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-MTAB-7497

ABSTRACT: TP53 is a master regulator of proteostasis in SMARCB1-deficient malignant rhabdoid tumors

PROVIDER: E-MTAB-7497 | ExpressionAtlas | 2019-03-20

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-MTAB-7497-analysis-methods.tsv	Tabular
	E-MTAB-7497-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-7497-configuration.xml	Xml
	E-MTAB-7497-percentile-ranks.tsv	Tabular
	E-MTAB-7497.condensed-sdrf.tsv	Tabular

Items per page:

1 - 5 of 40

Similar Datasets

Inactivation of p21-Activated Kinase 2 (Pak2) Inhibits the Development of Nf2-Deficient Tumors by Restricting Downstream Hedgehog and Wnt Signaling

Project description:Since loss of the NF2 tumor suppressor gene results in p21-activated kinase (Pak) activation, PAK inhibitors hold promise for the treatment of NF2-deficient tumors. To test this possibility, we asked if loss of Pak2, a highly expressed group I PAK member, affects the development of malignant mesothelioma in Nf2;Cdkn2a-deficient (NC) mice and the growth properties of NC mesothelioma cells in culture. In vivo, deletion of Pak2 resulted in a markedly decreased incidence and delayed onset of both pleural and peritoneal malignant mesotheliomas in NC mice. In vitro, Pak2 deletion decreased malignant mesothelioma cell viability, migration, clonogenicity, and spheroid formation. RNA-seq analysis demonstrated downregulated expression of Hedgehog and Wnt pathway genes in NC;Pak2-/- mesothelioma cells versus NC;Pak2+/+ mesothelioma cells. Targeting of the Hedgehog signaling component Gli1 or its target gene Myc inhibited cell viability and spheroid formation in NC;P+/+ mesothelioma cells. Kinome profiling uncovered kinase changes indicative of EMT in NC;Pak2-/- mesothelioma cells, suggesting that Pak2-deficient malignant mesotheliomas can adapt by reprogramming their kinome in the absence of Pak activity. The identification of such compensatory pathways offers opportunities for rational combination therapies to circumvent resistance to anti-PAK drugs.

2023-03-10 | PXD030571 | Pride

NR2F2 controls malignant squamous cell carcinoma state by promoting stemness and invasion and repressing differentiation IV

Project description:The non-genetic mechanisms required to sustain malignant tumor state are poorly understood. During the transition from benign tumors to malignant carcinoma, tumor cells need to repress differentiation and acquire invasive features. Using transcriptional profiling of cancer stem cells (CSC) from benign tumors and malignant skin squamous cell carcinoma (SCC), we identified the nuclear receptor NR2F2 as uniquely expressed in malignant SCC. Using genetic gain- and loss-of-function in vivo, we show that NR2F2 is essential for promoting the malignant tumor state by controlling tumor stemness and maintenance in mouse and human SCC. We demonstrate that NR2F2 promotes tumor cell proliferation, epithelial-mesenchymal transition (EMT) and invasive features, while repressing tumor differentiation and immune cell infiltration by regulating a common transcriptional program in mouse and human SCCs. Altogether, we identify NR2F2 as a key regulator of malignant CSC functions that promotes tumor renewal and restricts differentiation to sustain malignant tumor state.

2021-09-27 | GSE175724 | GEO

Immunogenomics of Malignant Brain Tumors

Project description:Immunogenomics of Malignant Brain Tumors

| PRJNA763945 | ENA

Immunogenomics of Malignant Brain Tumors

Project description:Immunogenomics of Malignant Brain Tumors

| PRJNA763970 | ENA

Study of Pembrolizumab (MK-3475) as Monotherapy in Participants With Previously-Treated Locally Advanced Unresectable or Metastatic Colorectal Cancer (MK-3475-164/KEYNOTE-164)

Project description:In this study, participants with previously-treated locally-advanced unresectable or metastatic mismatched repair (MMR) deficient or microsatellite instability-high (MSI-H) colorectal carcinoma (CRC) will be treated with pembrolizumab (MK-3475, KEYTRUDA) monotherapy. There will be two cohorts in this study: Cohort A and Cohort B. For Cohort A, participants are required to have been previously treated with standard therapies, which must include fluoropyrimidine, oxaliplatin, and irinotecan. Enrollment into Cohort A has been completed. For Cohort B, participants are required to have been previously treated with at least one line of systemic standard of care therapy: fluoropyrimidine + oxaliplatin or fluoropyrimidine + irinotecan +/ - anti-vascular endothelial growth factor (VEGF)/ epidermal growth factor regulator (EGFR) monoclonal antibody. The primary hypothesis is that Objective Response Rate (ORR) based on Response Evaluation Criteria in Solid Tumors v 1.1 (RECIST 1.1) assessed by central imaging vendor in participants with locally advanced unresectable or metastatic MMR deficient or MSI high CRC is greater than 15%.

| 2191248 | ecrin-mdr-crc

HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers [ChIP-Seq]

Project description:Heat-Shock Factor 1 (HSF1), master regulator of the heat-shock response, facilitates malignant transformation, cancer cell survival and proliferation in model systems. The common assumption is that these effects are mediated through regulation of heat-shock protein (HSP) expression. However, the transcriptional network that HSF1 coordinates directly in malignancy and its relationship to the heat-shock response have never been defined. By comparing cells with high and low malignant potential alongside their non-transformed counterparts, we identify an HSF1-regulated transcriptional program specific to highly malignant cells and distinct from heat shock. Cancer-specific genes in this program support oncogenic processes: cell-cycle regulation, signaling, metabolism, adhesion and translation. HSP genes are integral to this program, however, even these genes are uniquely regulated in malignancy. This HSF1 cancer program is active in breast, colon and lung tumors isolated directly from human patients and is strongly associated with metastasis and death. Thus, HSF1 rewires the transcriptome in tumorigenesis, with prognostic and therapeutic implications. ChIP-seq was used to characterize HSF1 binding

2012-08-07 | E-GEOD-38901 | biostudies-arrayexpress

Mus musculus

Project description:Rb1 deficient Apc1638N cecal tumors vs duodenal tumors

| PRJNA109869 | ENA

NR2F2 is an essential regulator of malignant tumor state by promoting tumor stemness, invasion and repressing differentiation I

2021-09-29 | GSE164592 | GEO

NR2F2 controls malignant squamous cell carcinoma state by promoting stemness and invasion and repressing differentiation III

2021-09-27 | GSE164602 | GEO

NR2F2 controls malignant squamous cell carcinoma state by promoting stemness and invasion and repressing differentiation II

2021-09-27 | GSE164597 | GEO